Herpes simplex virus type I induces the accumulation of intracellular β-amyloid in autophagic compartments and the inhibition of the non-amyloidogenic pathway in human neuroblastoma cells
| العنوان: | Herpes simplex virus type I induces the accumulation of intracellular β-amyloid in autophagic compartments and the inhibition of the non-amyloidogenic pathway in human neuroblastoma cells |
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| المؤلفون: | Soraya Santana, Jesús Aldudo, Fernando Valdivieso, María J. Bullido, María Recuero |
| المساهمون: | Ministerio de Educación y Ciencia (España), Obra social Caja de Ahorros y Monte de Piedad de Madrid, Comunidad de Madrid, Ministerio de Sanidad y Consumo (España), Asociación Nacional del Alzhéimer (España), Fundación Ramón Areces |
| المصدر: | Digital.CSIC. Repositorio Institucional del CSIC instname |
| بيانات النشر: | Elsevier, 2012. |
| سنة النشر: | 2012 |
| مصطلحات موضوعية: | Aging, Amyloidogenic Proteins, Herpesvirus 1, Human, Neuroblastoma, Lysosome, Cell Line, Tumor, Amyloid precursor protein, medicine, Autophagy, Humans, Secretion, Amyloid beta-Peptides, biology, General Neuroscience, P3 peptide, HSV-1, Cell biology, medicine.anatomical_structure, B-amyloid, Amyloidogenic pathway, Biochemistry, biology.protein, Neurology (clinical), Geriatrics and Gerontology, Signal transduction, App, Amyloid precursor protein secretase, Alzheimer’s disease, Intracellular, Developmental Biology, Signal Transduction |
| الوصف: | Mounting evidence suggests that herpes simplex virus type 1 (HSV-1) is involved in the pathogenesis of Alzheimer's disease (AD). Epidemiological analyses have shown that HSV-1 is a risk factor for AD in people with at least 1 type 4 allele of the apolipoprotein E gene. Recent studies have also suggested that HSV-1 contributes to the appearance of the biochemical anomalies characteristic of AD brains. In addition, autophagic activity appears to be reduced with aging, and the final stages of autophagy in neurodegenerative process appear to be impaired. The present work reports that HSV-1 provokes the strong intracellular accumulation of both the main species of β-amyloid (Aβ) in the autophagic compartments and that it is associated with a marked inhibition of Aβ secretion. Autophagosomes containing Aβ failed to fuse with lysosomes in HSV-1-infected cells, indicating the impaired degradation of Aβ localized in the autophagic vesicles. In addition, HSV-1 infection was associated with the inhibition of the nonamyloidogenic pathway of amyloid precursor protein (APP) processing without significantly affecting the activity of the secretases involved in the amyloidogenic pathway. Taken together, these data suggest that HSV-1 infection modulates autophagy and amyloid precursor protein processing, contributing to the accumulation of Aβ characteristic of AD. © 2012 Elsevier Inc. Ministerio de Educación y Ciencia (GEN2003-20235-C05-05); Obra Social Caja Madrid; Comunidad Autónoma de Madrid (GR/SAL/0783/2004); Ministerio de Sanidad y Consumo (Instituto de Salud Carlos III); Asociación de Familiares de Enfermos de Alzheimer (AFAL); Fundación Ramón Areces |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::435ad3f7db353f3c5047f83c6652bdfa http://hdl.handle.net/10261/113230 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....435ad3f7db353f3c5047f83c6652bdfa |
| قاعدة البيانات: | OpenAIRE |
| الوصف غير متاح. |